ArticleMolecular microbiology2009
The BosR regulatory protein of Borrelia burgdorferi interfaces with the RpoS regulatory pathway and modulates both the oxidative stress response and pathogenic properties of the Lyme disease spirochete.
Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
103 citing papers in PubMed, 126 citations in OpenAlex.
- mGem: A tale as old as blood-do tick-borne pathogens exploit arthropod antioxidant defenses?mBio · 2026Review
- TheInfection and immunity · 2026Article
- DNA Binding by BosR Controls RpoS-Dependent and -Independent Gene Expression in Borrelia burgdorferi.Molecular microbiology · 2026Article
- The BosR Is Back!Molecular microbiology · 2026Article
- Virulence Regulation inMicroorganisms · 2025Review
- Article
- Borrelia burgdorferi serine protease HtrA is a pleiotropic regulator of stress response, motility, flagellar hemostasis, and infectivity.Communications biology · 2025Article
- Analysis of the BadR regulon in Borrelia burgdorferi.BMC microbiology · 2025Article
- Article
- Analysis of bb0556 Expression and Its Role During Borrelia burgdorferi Mammalian Infection.Molecular microbiology · 2024Article
- Hitchhiker's Guide toJournal of bacteriology · 2024Review
- Positive feedback regulation between RpoS and BosR in the Lyme disease pathogen.bioRxiv : the preprint server for biology · 2024Article
- A Fur family protein BosR is a novel RNA-binding protein that controls rpoS RNA stability in the Lyme disease pathogen.Nucleic acids research · 2024Article
- Article
- The Lyme disease spirochete, Borrelia burgdorferi, as a model vector-borne pathogen: insights on regulation of gene and protein expression.Current opinion in microbiology · 2023Review
- PERK-mediated antioxidant response is key for pathogen persistence in ticks.bioRxiv : the preprint server for biology · 2023Article
- Chemotaxis Coupling Protein CheWInfection and immunity · 2023Article
- Role of the Hypothetical Protein BB0563 during Borrelia burgdorferi Infection in Animals.Infection and immunity · 2023Article
- Article
- The Consistent Tick-Vertebrate Infectious Cycle of the Lyme Disease Spirochete Enables Borrelia burgdorferi To Control Protein Expression by Monitoring Its Physiological Status.Journal of bacteriology · 2022Review
43 more citing papers are in PubMed but not listed here.
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Summary Borrelia burgdorferi, the Lyme disease spirochete, adapts as it moves between the arthropod and mammalian hosts that it infects. We hypothesize that BosR serves as a global regulator in B. burgdorferi to modulate the oxidative stress response and adapt to mammalian hosts. To test this hypothesis, a bosR mutant in a low-passage B. burgdorferi isolate was constructed. The resulting bosR::kan(R) strain was altered when grown microaerobically or anaerobically suggesting that BosR is required for optimal replication under both growth conditions. The absence of BosR increased the sensitivity of B. burgdorferi to hydrogen peroxide and reduced the synthesis of Cdr and NapA, proteins important for cellular redox balance and the oxidative stress response, respectively, suggesting an important role for BosR in borrelial oxidative homeostasis. For the bosR mutant, the production of RpoS was abrogated and resulted in the loss of OspC and DbpA, suggesting that BosR interfaces with the Rrp2-RpoN-RpoS regulatory cascade. Consistent with the linkage to RpoS, cells lacking bosR were non-infectious in the mouse model of infection. These results indicate that BosR is required for resistance to oxidative stressors and provides a regulatory response that is necessary for B. burgdorferi pathogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.